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Updated: May 6, 2026
A Swine Model of Neonatal Asphyxia
Published on: October 11, 2011
Normoxic Versus Hyperoxic Management of Blunt Traumatic Brain Injury at Ground Level and During Simulated Aeromedical
Yanyi Zang1, Teryn R Roberts1, Brendan M Beely1
1Autonomous Reanimation and Evacuation Research Institute, The Geneva Foundation, San Antonio, TX 78235, United States.
Background:
Aeromedical evacuation (AE) environments are characterized by hypobaria and may cause secondary insult to casualties with traumatic brain injury (TBI). As increased FiO2 is commonly administered to mechanically ventilated casualties during AE, it may exacerbate TBI. We hypothesized that hyperoxia at ground level and/or during simulated AE worsens neuroinflammation and neurodegeneration after mild-to-moderate blunt TBI.
Materials And Methods:
Female Yorkshire swine were anesthetized, mechanically ventilated, and received blunt TBI via a modified humane stunner. Animals were randomized into 1 of 4 groups (n = 8/group): Ground Normoxia (G-Norm); Ground Hyperoxia (G-Hyper); AE Normoxia (AE-Norm); and AE Hyperoxia (AE-Hyper), with AE groups placed in a hypobaric chamber for 6 hours at 8,000 ft and then managed in an ICU for 24 hours. Neuroinflammation and neurodegeneration were assessed via histological injury scores (0 = no injury, and 4 = most severe injury), as well as measurements of systemic HMGB1, S100β, GFAP, and cytokines such as IL-1β, IL-6, and IL-10 levels. In addition, we assessed hemodynamics, intracranial pressure, blood gases and chemistry, and coagulation variables.
Results:
TBI led to increased intracranial pressure, tachycardia, and transient hypertension with subsequent periodic fluctuations in heart rate and blood pressure. The G-Norm and G-Hyper groups had mild-to-moderate injuries (cerebrum: 2.0 and 1.75, respectively, NS; brainstem: 2.0 and 1.71, respectively, NS). The AE-Norm and AE-Hyper groups had numerically less injuries (cerebrum: 1.5 and 1.71, respectively, NS; brainstem: 0.86 and 1.25, respectively, NS). HMGB1 increased 2-fold after TBI in all 4 groups (P<.003). IL-6 increased after TBI and remained elevated relative to baseline in all groups except AE-Hyper group (P<.0001). No within or between-group differences were observed in any other variables.
Conclusions:
This 24-hour intent-to-treat study did not identify discernable differences in normoxic versus hyperoxic management of TBI at ground level or during AE. Future studies should evaluate exposures to hypobaria and hyperoxia over longer durations.
